摘要
目的探讨外源性及内源性二氧化硫(SO2)对低氧性肺动脉高压(HPH)模型中炎性反应的影响。方法将Wistar大鼠随机分为4组:对照组(n=8)、低氧组(n=8)、低氧加SO2组(n=10,予外源性SO2供体Na2SO3/NaHSO3)和低氧加天冬氨酸异羟肟酸(HDX)组(n=10,予内源性SO2生成酶抑制剂HDX)。对低氧组、低氧加SO2组和低氧加HDX组大鼠予低氧处理21d,对照组大鼠置常氧环境。检测各组大鼠肺动脉平均压、肺组织匀浆中SO2水平,免疫组织化学法检测其肺小动脉内皮细胞核转录因子(NF)-κB和细胞间黏附因子-1(ICAM-1)表达情况。结果与对照组比较,低氧组大鼠肺动脉平均压升高127.13%(P<0.01),其肺组织匀浆中SO2水平降低42.64%(P<0.01),肺小动脉内皮细胞NF-κB表达阳性百分比升高303.47%(P<0.01),ICAM-1表达升高119.25%(P<0.01);与低氧组比较,低氧加SO2组大鼠肺动脉平均压降低15.09%(P<0.05),肺组织匀浆中SO2水平升高40.54%(P<0.01),内皮细胞NF-κB表达阳性百分比降低37.71%(P<0.01),ICAM-1表达降低13.65%(P<0.01);与低氧组比较,低氧加HDX组大鼠肺动脉平均压升高13.58%(P<0.01),肺组织匀浆中SO2水平降低40.54%(P<0.01),内皮细胞NF-κB表达阳性百分比升高22.18%(P<0.01),ICAM-1表达升高11.92%(P<0.01)。结论SO2在HPH炎性反应形成过程中发挥重要的保护性调节作用。
Objective To explore the effect of exogenous and endogenous sulfur dioxide （ SO2 ） on small pulmonary artery endothelial cell inflammation reaction in pathogenesis of hypoxic pulmonary hypetension （ HPH ）. Methods Wistar rats were randomly divided into 4 groups ： control group （ n = 8 ）, hypoxic group （ n = 8 ）, hypoxic plus SO2 group （ n = 10, given Na2 SO3/NaHSO3 ） and hypoxic plus hydroxamate （HDX） group （n = 10, given HDX）. The rats of hypoxic group ,hypoxic plus SO2 group and hypoxic plus HDX group had been under a hypoxic condition for 21 days,while control group had been under room air. The mean pulmonary artery pressure ,the content of SO2 in lung tissue, the expression of nuclear factor - kappa B （ NF - KB ） and intracellular adhesion molecule - 1 （ ICAM - 1 ） were investigated and analyzed.-Resuits Compared with control group, mean pulmonary artery pressure of hypoxic group raised by 127.13 % （P 〈 0.01 ）, the content of SO2 in lung tissue descended by 42.64% （P 〈0.01 ）, the expression of NF - KB raised by 303.47% （ P 〈 0.01 ）, and the expression of ICAM - 1 raised by 119.25 % （P 〈 0.01 ） ;whereas compared with hypoxic group, mean pulmonary artery pressure of hypoxic plus SO2 group descended by 15.09% （ P 〈 0.01 ）, the content of SO2 in lung tissue raised by 40.54% （ P 〈 0.01 ）, the expression of NF - KB descended by 37.71% （ P 〈 0.01 ）, and the expression of ICAM - 1 descended by 13.65 % （ P 〈 0.01 ） ; compared with hypoxic group, mean pulmonary artery pressure of hypoxic plus HDX group raised by 13.58% （ P 〈 0.01 ）, the content of SO2 in lung tissue descended by 40.54% （ P 〈 0.01 ）, the expression of NF - KB raised by 22.18% （ P 〈 0.01 ）, and the expression of ICAM - 1 raised by 11.92% （ P 〈 0.01 ）. Conclusions SO2 play an important preventive role in protecting and regulating inflammation of experimental HPH in rats.
出处
《实用儿科临床杂志》
CAS
CSCD
北大核心
2008年第13期985-987,990,共4页
Journal of Applied Clinical Pediatrics
基金
国家长江学者奖励计划
国家杰出青年科学基金项目资助(30425010)
国家自然科学基金项目资助(30571971)
国家自然科学基金重点项目资助(30630031)
